Heart failure refers to the heart's inability to keep up with the demands made upon it. Congestive heart failure refers to an inability of the heart to pump an adequate amount of blood to the body tissues. Because the heart is unable to pump an adequate amount of blood, blood returning to the heart becomes congested in the venous system.
In a healthy heart, the heart pumps all of the blood that returns to it, according to the Frank-Starling law. Increased venous return leads to increased end diastolic volume, which causes increased strength of contraction and increased stroke volume. In addition to intrinsic control according to the Frank-Starling law, a healthy heart is subject to extrinsic control, such as stimulation by the sympathetic nervous system to enhance contractility.
In a patient experiencing congestive heart failure, intrinsic and extrinsic control mechanisms may not function properly, and consequently the heart may fail to pump an adequate amount of blood. A condition known as cardiac decompensation is used to describe heart failure that results in a failure of adequate circulation.
Failure of the left side of the heart is generally more serious than the failure of the right side. On the left side of the heart, blood returns from the pulmonary system and is pumped to the rest of the body. When the left side of the heart fails, there are consequences to both the pulmonary system and to the rest of the body. A patient with congestive heart failure may be unable to pump enough blood forward to provide an adequate flow of blood to his kidneys, for example, causing him to retain excess water and salt. His heart may also be unable to handle the blood returning from his pulmonary system, resulting in a damming of the blood in the lungs and increasing his risk of developing pulmonary edema.
Causing more blood to be expelled from the heart, i.e., increasing cardiac output would reduce the damming of blood in the lungs and the congestion of blood in the venous system caused by heart failure. In addition to pharmacological therapies to increase cardiac output, some patients with congestive heart failure benefit from an implanted pacemaker. A pacemaker rhythmically generates pacing pulses that spread throughout the heart to drive the atria and ventricles. A typical pacemaker monitors the electrical activity of the patient's heart and provides pacing pulses to cause the heart to beat at a desired rate, such as sixty beats per minute. Because cardiac output depends in part on heart rate, increasing the pacing rate of a pacemaker has been used as a method of increasing cardiac output.
Existing methods for increasing or optimizing cardiac output may involve modulation of a variety of parameters associated with a pacing program other than the pacing rate. For example, some existing methods modulate atrial escape interval, atrioventricular (A-V) delay, sequential mode of operation, refractory period, pacing pulse energy, pulse amplitude, or pulse width, which is sometime referred to as pulse duration. The energy level of a pacing pulse is a function of several parameters, including pulse amplitude and pulse width.
For example, Nakayama, et. al., “High Output Ventricular Pacing Increased the Cardiac Output,” EUR.J.C.P.E., Vol. 6, No. 1, June 1996, reported that high voltage amplitude ventricular pacing increased cardiac output as measured by Doppler echocardiogram and cardio-thoracic ratio. Cardiac output was higher when paced at high voltage amplitude, 4.2 or 5.0 volts, than at low voltage amplitude, 2.5 volts. Nakayama, et. al., concluded that the increase in cardiac output was due to the synchronous contraction of the ventricle caused by a larger field stimulation area due to high voltage pacing.
Because the condition of a patient may change between visits to a physician, and because the patients need for increased cardiac output may also vary as a result of the demand caused by the patient's activity, it is desirable to monitor the patient's need for increased cardiac output continuously. Some existing methods use implanted devices that can estimate cardiac output and control a pacemaker to modulate pacing parameters to maximize cardiac output in a feedback mechanism. For example, U.S. Pat. No. 5,891,176, issued to Bornzin, discloses measuring mixed venous oxygen saturation, blood flow, or ventricular pressure as an estimate of cardiac output, and modulating pacing parameters such as atrial escape interval, A-V delay, and sequential mode of operation to maximize mixed venous oxygen saturation, blood flow, or ventricular pressure. U.S. Pat. No. 6,314,323, issued to Elkwall, discloses integrating a measured ventricular pressure curve during systole, using the integration result as an estimate of cardiac output, and modulating pacing parameters such as A-V delay, stimulation rate, refractory period, stimulation pulse energy, duration and amplitude to maximize the integrated value. These existing methods, however, may not accurately estimate the need for increased cardiac output, or may require complicated devices and methods to estimate the need for increased cardiac output. These problems may cause less effective treatment of the symptoms of cardiac decompensation, or may increase complexity, expense, and power consumption of an implantable device.
Examples of the above referenced existing techniques and/or devices may be found in the issued U.S. Patents listed in Table 1 below.
TABLE 1U.S. Pat. No.InventorIssue Date6,314,323ElkwallNov. 6, 20015,891,176BornzinApr. 6, 19995,626,623Kieval et al.May 6, 19975,368,040CarneyNov. 29, 1994
All patents listed in Table 1 above are hereby incorporated by reference herein in their respective entireties. As those of ordinary skill in the art will appreciate readily upon reading the Summary of the Invention, Detailed Description of the Preferred Embodiments and claims set forth below, many of the devices and methods disclosed in the patents of Table 1 may be modified advantageously by using the techniques of the present invention.